ArticleJournal of thoracic disease2022
Myocardial protective effect of sivelestat sodium in rat models with sepsis-induced myocarditis.
Article in Journal of thoracic disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Therapeutic effect and mechanism of sivelestat sodium on acute lung injury: A randomized controlled trial.Medicine · 2025Trial
- MiR-143-5p serves as a diagnostic biomarker in patients with sepsis and regulates sepsis-induced inflammation and cardiac dysfunction.Hereditas · 2025Article
- The Protective Effects of Sivelestat Sodium on the Basis of Corticosteroid Therapy in Patients With Moderate-to-Severe Acute Respiratory Distress Syndrome.Emergency medicine international · 2025Article
- Effect of sivelestat sodium on the incidence of ventilator-associated pneumonia in patients with sepsis and ARDS.Frontiers in medicine · 2025Article
- A novel biomarker of COVID-19: MMP8 emerged by integrated bulk RNAseq and single-cell sequencing.Scientific reports · 2024Article
- Sivelestat sodium alleviated sepsis-induced acute lung injury by inhibiting TGF-β/Smad signaling pathways through upregulating microRNA-744-5p.Journal of thoracic disease · 2024Article
- The beneficial effects of neutrophil elastase inhibitor on gastrointestinal dysfunction in sepsis.Clinical and translational science · 2024Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The incidence of sepsis has been steadily increasing worldwide, and the heart is one of the target organs that can be easily damaged by sepsis. At present, antibiotics and organ function support are the main treatment options for sepsis and multiple system organ dysfunction, but are still under investigation. Methods: Fifty rats were randomly divided into the sham operation group, sepsis group, sivelestat sodium low-dose (L) group (administered with sivelestat sodium 1.6 mg/kg), sivelestat sodium middle-dose (M) group (administered with sivelestat sodium 4.8 mg/kg), and sivelestat sodium high-dose (H) group (administered with sivelestat sodium 10 mg/kg). Morphological changes of myocardial cells and the distribution of extracellular signal-regulated kinase (ERK)1/2 proteins were observed by light microscope. Serum troponin-T, creatine kinase isoenzyme MB, brain natriuretic peptide, interleukin (IL)-6, tumor necrosis factor-α, and IL-1β levels and changes in cardiac function indicators were measured. The protein expressions of Bax, Bcl-2, and ERK1/2 were detected by Western blotting. Results: Compared with the sham operation group, the release of inflammatory factors in the sepsis group increased; the protein expressions of Bax, Bcl-2, and ERK1/2 increased; left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), and maximum rate of LVP rise (+dp/dtmax) level decreased, whereas -dp/dtmax increased. In the sivelestat sodium groups, the release of inflammatory factors decreased; Bax expression decreased, whereas Bcl-2 and ERK1/2 protein expressions increased; LVSP, LVEDP, and +dp/dtmax increased, whereas -dp/dtmax decreased. In addition, all of these changes occurred in a dose-dependent manner. Conclusions: Sivelestat sodium can effectively lower the expressions of inflammatory factors and improve cardiac function. It can act on the ERK1/2 signaling pathway to exert its cardiomyocyte-protective effect, and the activation of this signaling pathway can offer potential treatment sites for septic myocarditis.
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